Abstract
Purpose: The trigeminal ganglion branches into three branches – the orbital, maxillary and mandibular nerves – with the peripheral ends distributing widely into the craniocervical region. Within the trigeminal ganglion, predilection in the localization of neurons can be observed, although the relationship between localization of these neurons and the region of innervation is unclear. In the present study, we visualized the neurons with neuronal marker ATF3 antibody (activating transcription factor 3 antibody) and comparatively examined the localization of these neurons.
Method: The rat trigeminal ganglion was extracted seven days after the administration of ATF3 (ATF3 expression is believed to peak after seven days) and the supraorbital, infraorbital, inferior alveolar, and lingual nerves were isolated, along with a control specimen in which no neurons were damaged. The specimens were sliced at a thickness of 100μm. The microscopic slides were stained with ATF3 antibody, NeuN antibody, which discriminately stains the nuclei of neurons, and DAPI antibody, which indiscriminately stains the nuclei of all cells. The stained slides were then observed under an optical microscope and sequential microscopic images were saved onto a hard drive and reconstructed three-dimensionally to recreate a 3D image of the trigeminal ganglion.
Result: The present study revealed that rat trigeminal ganglion consists of two parts; the first and the second branches comprising one, and the third branch sprouting outward from the first two branches comprising the second part. Likewise, the localization of neurons was evident in the rostral and caudal regions. These two regions of innervations were fused in the dorsal area and separated in the abdominal area. Examination of ATF3- and NeuN-positive neurons revealed that following the scission of the supraorbital nerve, the localization of ATF3 neurons were observed medially in the rostral region, whereas the localization of ATF3 neurons were observed throughout the entire rostral region following the scission of the infraorbital nerve. Following the scission of the inferior alveolar nerve, localization of ATF-positive neurons was mainly observed in the dorsal region, and scattered at the rostral-dorsal junction. Scission of the lingual nerve resulted in a similar pattern of localization as observed following the scission of the inferior alveolar nerve. Simultaneous scission of the infraorbital, inferior alveolar, and lingual nerves resulted in intermixed localization of ATF3-positive neurons, making the innervations of these nerves undistinguishable.
Conclusion: Theories exist that damaged neurons within the rat trigeminal ganglion which are adjacent to undamaged neurons transmit a form of neurotransmitter (yet to be identified in the current study) that may be responsible for the onset of ectopic allodynia. We believe that our present study will present an explanation for the mechanisms behind the onset of ectopic allodynia.
